Impaired lymphocyte development and antibody class switching and increased malignancy in a murine model of DNA ligase IV syndrome.

@article{Nijnik2009ImpairedLD,
  title={Impaired lymphocyte development and antibody class switching and increased malignancy in a murine model of DNA ligase IV syndrome.},
  author={Anastasia Nijnik and Sara J. Dawson and Tanya L. Crockford and Lisa J Woodbine and Supawan Visetnoi and Sophia Bennett and Margaret D. Jones and Gareth D. H. Turner and Penelope A. Jeggo and Christopher C. Goodnow and Richard J. Cornall},
  journal={The Journal of clinical investigation},
  year={2009},
  volume={119 6},
  pages={1696-705}
}
Hypomorphic mutations in DNA ligase IV (LIG4) cause a human syndrome of immunodeficiency, radiosensitivity, and growth retardation due to defective DNA repair by the nonhomologous end-joining (NHEJ) pathway. Lig4-null mice are embryonic lethal, and better mouse models are needed to study human LigIV syndrome. We recently identified a viable mouse strain with a Y288C hypomorphic mutation in the Lig4 gene. Lig4Y288C mice exhibit a greater than 10-fold reduction of LigIV activity in vivo and… CONTINUE READING

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Hypomorphic mutations in DNA ligase IV ( LIG4 ) cause a human syndrome of immunodeficiency , radiosensitivity , and growth retardation due to defective DNA repair by the nonhomologous end - joining ( NHEJ ) pathway .
Hypomorphic mutations in DNA ligase IV ( LIG4 ) cause a human syndrome of immunodeficiency , radiosensitivity , and growth retardation due to defective DNA repair by the nonhomologous end - joining ( NHEJ ) pathway .
LIG4 protein, humanGene product plays role in biological processNon-Homologous DNA End-Joining
Hypomorphic mutations in DNA ligase IV ( LIG4 ) cause a human syndrome of immunodeficiency , radiosensitivity , and growth retardation due to defective DNA repair by the nonhomologous end - joining ( NHEJ ) pathway .
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